Chtn Bibliography
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Supplementary Data
Supplementary Data for Quantitative Changes in the Mitochondrial Proteome from Subjects with Mild Cognitive Impairment, Early Stage and Late Stage Alzheimer’s disease Table 1 - 112 unique, non-redundant proteins identified and quantified in at least two of the three analytical replicates for all three disease stages. Table 2 - MCI mitochondrial samples, Protein Summary Table 3 - MCI mitochondrial samples, Experiment 1 Table 4 - MCI mitochondrial samples, Experiment 2 Table 5 - MCI mitochondrial samples, Experiment 3 Table 6 - EAD Mitochondrial Study, Protein Summary Table 7 - EAD Mitochondrial Study, Experiment 1 Table 8 - EAD Mitochondrial Study, Experiment 2 Table 9 - EAD Mitochondrial Study, Experiment 3 Table 10 - LAD Mitochondrial Study, Protein Summary Table 11 - LAD Mitochondrial Study, Experiment 1 Table 12 - LAD Mitochondrial Study, Experiment 2 Table 13 - LAD Mitochondrial Study, Experiment 3 Supplemental Table 1. 112 unique, non-redundant proteins identified and quantified in at least two of the three analytical replicates for all three disease stages. Description Data MCI EAD LAD AATM_HUMAN (P00505) Aspartate aminotransferase, mitochondrial precursor (EC Mean 1.43 1.70 1.31 2.6.1.1) (Transaminase A) (Glutamate oxaloacetate transaminase 2) [MASS=47475] SEM 0.07 0.09 0.09 Count 3.00 3.00 3.00 ACON_HUMAN (Q99798) Aconitate hydratase, mitochondrial precursor (EC 4.2.1.3) Mean 1.24 1.61 1.19 (Citrate hydro-lyase) (Aconitase) [MASS=85425] SEM 0.05 0.17 0.18 Count 3.00 2.00 3.00 ACPM_HUMAN (O14561) Acyl carrier protein, mitochondrial -
Olig1 and Sox10 Interact Synergistically to Drivemyelin Basic
The Journal of Neuroscience, December 26, 2007 • 27(52):14375–14382 • 14375 Cellular/Molecular Olig1 and Sox10 Interact Synergistically to Drive Myelin Basic Protein Transcription in Oligodendrocytes Huiliang Li,1 Yan Lu,2 Hazel K. Smith,1 and William D. Richardson1 1Wolfson Institute for Biomedical Research and Department of Biology, University College London, London WC1E 6BT, United Kingdom, and 2Medical Research Council, Clinical Sciences Centre, Imperial College London, London W12 0NN, United Kingdom The oligodendrocyte lineage genes (Olig1/2), encoding basic helix-loop-helix transcription factors, were first identified in screens for master regulators of oligodendrocyte development. OLIG1 is important for differentiation of oligodendrocyte precursors into myelin- forming oligodendrocytes during development and is thought to play a crucial role in remyelination during multiple sclerosis. However, itisstillunclearhowOLIG1interactswithitstranscriptionalcofactorsandDNAtargets.OLIG1wasreportedlyrestrictedtomammals,but we demonstrate here that zebrafish and other teleosts also possess an OLIG1 homolog. In zebrafish, as in mammals, Olig1 is expressed in the oligodendrocyte lineage. Olig1 associates physically with another myelin-associated transcription factor, Sox10, and the Olig1/Sox10 complex activates mbp (myelin basic protein) transcription via conserved DNA sequence motifs in the mbp promoter region. In contrast, Olig2 does not bind to Sox10 in zebrafish, although both OLIG1 and OLIG2 bind SOX10 in mouse. Key words: Olig1; Olig2; Sox10; Mbp; oligodendrocyte; myelin; zebrafish; mouse; evolution; development Introduction directly regulates Mbp transcription (Stolt et al., 2002), and over- Myelin, the multilayered glial sheath around axons, is one of the expression of SOX10 alone is sufficient to induce myelin gene defining features of jawed vertebrates (gnathostomes). It is expression in embryonic chick spinal cord (Liu et al., 2007). -
Data Sheet Cathepsin V Inhibitor Screening Assay Kit Catalog #79589 Size: 96 Reactions
6405 Mira Mesa Blvd Ste. 100 San Diego, CA 92121 Tel: 1.858.202.1401 Fax: 1.858.481.8694 Email: [email protected] Data Sheet Cathepsin V Inhibitor Screening Assay Kit Catalog #79589 Size: 96 reactions BACKGROUND: Cathepsin V, also called Cathepsin L2, is a lysosomal cysteine endopeptidase with high sequence homology to cathepsin L and other members of the papain superfamily of cysteine proteinases. Its expression is regulated in a tissue-specific manner and is high in thymus, testis and cornea. Expression analysis of cathepsin V in human tumors revealed widespread expression in colorectal and breast carcinomas, suggesting a possible role in tumor processes. DESCRIPTION: The Cathepsin V Inhibitor Screening Assay Kit is designed to measure the protease activity of Cathepsin V for screening and profiling applications. The Cathepsin V assay kit comes in a convenient 96-well format, with purified Cathepsin V, its fluorogenic substrate, and Cathepsin buffer for 100 enzyme reactions. In addition, the kit includes the cathepsin inhibitor E- 64 for use as a control inhibitor. COMPONENTS: Catalog # Component Amount Storage 80009 Cathepsin V 10 µg -80 °C Fluorogenic Cathepsin Avoid 80349 Substrate 1 (5 mM) 10 µl -20 °C multiple *4X Cathepsin buffer 2 ml -20 °C freeze/thaw E-64 (1 mM) 10 µl -20 °C cycles! 96-well black microplate * Add 120 µl of 0.5 M DTT before use. MATERIALS OR INSTRUMENTS REQUIRED BUT NOT SUPPLIED: 0.5 M DTT in aqueous solution Adjustable micropipettor and sterile tips Fluorescent microplate reader APPLICATIONS: Great for studying enzyme kinetics and screening small molecular inhibitors for drug discovery and HTS applications. -
Genome-Wide DNA Methylation Analysis of KRAS Mutant Cell Lines Ben Yi Tew1,5, Joel K
www.nature.com/scientificreports OPEN Genome-wide DNA methylation analysis of KRAS mutant cell lines Ben Yi Tew1,5, Joel K. Durand2,5, Kirsten L. Bryant2, Tikvah K. Hayes2, Sen Peng3, Nhan L. Tran4, Gerald C. Gooden1, David N. Buckley1, Channing J. Der2, Albert S. Baldwin2 ✉ & Bodour Salhia1 ✉ Oncogenic RAS mutations are associated with DNA methylation changes that alter gene expression to drive cancer. Recent studies suggest that DNA methylation changes may be stochastic in nature, while other groups propose distinct signaling pathways responsible for aberrant methylation. Better understanding of DNA methylation events associated with oncogenic KRAS expression could enhance therapeutic approaches. Here we analyzed the basal CpG methylation of 11 KRAS-mutant and dependent pancreatic cancer cell lines and observed strikingly similar methylation patterns. KRAS knockdown resulted in unique methylation changes with limited overlap between each cell line. In KRAS-mutant Pa16C pancreatic cancer cells, while KRAS knockdown resulted in over 8,000 diferentially methylated (DM) CpGs, treatment with the ERK1/2-selective inhibitor SCH772984 showed less than 40 DM CpGs, suggesting that ERK is not a broadly active driver of KRAS-associated DNA methylation. KRAS G12V overexpression in an isogenic lung model reveals >50,600 DM CpGs compared to non-transformed controls. In lung and pancreatic cells, gene ontology analyses of DM promoters show an enrichment for genes involved in diferentiation and development. Taken all together, KRAS-mediated DNA methylation are stochastic and independent of canonical downstream efector signaling. These epigenetically altered genes associated with KRAS expression could represent potential therapeutic targets in KRAS-driven cancer. Activating KRAS mutations can be found in nearly 25 percent of all cancers1. -
Felipe Jun Fuzita Molecular Physiology of Digestion In
FELIPE JUN FUZITA MOLECULAR PHYSIOLOGY OF DIGESTION IN ARACHNIDA: FUNCTIONAL AND COMPARATIVE-EVOLUTIONARY APPROACHES Thesis presented to the Programa de Pós-Graduação Interunidades em Biotecnologia USP/Instituto Butantan/IPT, to obtain the Title of Doctor in Biotechnology. São Paulo 2014 FELIPE JUN FUZITA MOLECULAR PHYSIOLOGY OF DIGESTION IN ARACHNIDA: FUNCTIONAL AND COMPARATIVE-EVOLUTIONARY APPROACHES Thesis presented to the Programa de Pós-Graduação Interunidades em Biotecnologia USP/Instituto Butantan/IPT, to obtain the Title of Doctor in Biotechnology. Concentration area: Biotechnology Advisor: Dr. Adriana Rios Lopes Rocha Corrected version. The original electronic version is available either in the library of the Institute of Biomedical Sciences and in the Digital Library of Theses and Dissertations of the University of Sao Paulo (BDTD). São Paulo 2014 DADOS DE CATALOGAÇÃO NA PUBLICAÇÃO (CIP) Serviço de Biblioteca e Informação Biomédica do Instituto de Ciências Biomédicas da Universidade de São Paulo © reprodução total Fuzita, Felipe Jun. Molecular physiology of digestion in Arachnida: functional and comparative-evolutionary approaches / Felipe Jun Fuzita. -- São Paulo, 2014. Orientador: Profa. Dra. Adriana Rios Lopes Rocha. Tese (Doutorado) – Universidade de São Paulo. Instituto de Ciências Biomédicas. Programa de Pós-Graduação Interunidades em Biotecnologia USP/IPT/Instituto Butantan. Área de concentração: Biotecnologia. Linha de pesquisa: Bioquímica, biologia molecular, espectrometria de massa. Versão do título para o português: Fisiologia molecular da digestão em Arachnida: abordagens funcional e comparativo-evolutiva. 1. Digestão 2. Aranha 3. Escorpião 4. Enzimologia 5. Proteoma 6. Transcriptoma I. Rocha, Profa. Dra. Adriana Rios Lopes I. Universidade de São Paulo. Instituto de Ciências Biomédicas. Programa de Pós-Graduação Interunidades em Biotecnologia USP/IPT/Instituto Butantan III. -
Crystal Structure of Cathepsin X: a Flip–Flop of the Ring of His23
st8308.qxd 03/22/2000 11:36 Page 305 Research Article 305 Crystal structure of cathepsin X: a flip–flop of the ring of His23 allows carboxy-monopeptidase and carboxy-dipeptidase activity of the protease Gregor Guncar1, Ivica Klemencic1, Boris Turk1, Vito Turk1, Adriana Karaoglanovic-Carmona2, Luiz Juliano2 and Dušan Turk1* Background: Cathepsin X is a widespread, abundantly expressed papain-like Addresses: 1Department of Biochemistry and v mammalian lysosomal cysteine protease. It exhibits carboxy-monopeptidase as Molecular Biology, Jozef Stefan Institute, Jamova 39, 1000 Ljubljana, Slovenia and 2Departamento de well as carboxy-dipeptidase activity and shares a similar activity profile with Biofisica, Escola Paulista de Medicina, Rua Tres de cathepsin B. The latter has been implicated in normal physiological events as Maio 100, 04044-020 Sao Paulo, Brazil. well as in various pathological states such as rheumatoid arthritis, Alzheimer’s disease and cancer progression. Thus the question is raised as to which of the *Corresponding author. E-mail: [email protected] two enzyme activities has actually been monitored. Key words: Alzheimer’s disease, carboxypeptidase, Results: The crystal structure of human cathepsin X has been determined at cathepsin B, cathepsin X, papain-like cysteine 2.67 Å resolution. The structure shares the common features of a papain-like protease enzyme fold, but with a unique active site. The most pronounced feature of the Received: 1 November 1999 cathepsin X structure is the mini-loop that includes a short three-residue Revisions requested: 8 December 1999 insertion protruding into the active site of the protease. The residue Tyr27 on Revisions received: 6 January 2000 one side of the loop forms the surface of the S1 substrate-binding site, and Accepted: 7 January 2000 His23 on the other side modulates both carboxy-monopeptidase as well as Published: 29 February 2000 carboxy-dipeptidase activity of the enzyme by binding the C-terminal carboxyl group of a substrate in two different sidechain conformations. -
SUPPLEMENTAL FIGURE LEGENDS Supplemental Figure S1. RBPJ
Xie et al. SUPPLEMENTAL FIGURE LEGENDS Supplemental Figure S1. RBPJ correlates with BTIC marker expression. A-D. The TCGA GBM dataset was downloaded and correlations analyzed by R. RBPJ mRNA levels were highly correlated with (A) Olig2, (B) Sox2, (C) CD133, and (D) Sox4 levels. E. RBPJ is preferentially expressed in proneural glioblastomas. The glioblastoma TCGA dataset was interrogated for RBPJ mRNA expression segregated by transcriptional profile. The proneural tumors were further divided into G-CIMP (glioma CpG-island methylator phenotype) or non-G-CIMP. **, p < 0.01. ****, p < 0.0001. *****, p < 0.00001. Supplemental Figure S2. Targeting RBPJ induces BTIC apoptosis. A. 3691 BTICs were transduced with shCONT, shRBPJ-1, or shRBPJ-2. Lysates were prepared and immunoblotted with the indicated antibodies. shRNA-mediated knockdown of RBPJ was associated with increased cleaved (activated) PARP. B. 3691 BTICs were transduced with shCONT, shRBPJ-1, or shRBPJ-2. Apoptosis measured by Annexin V staining. Data are presented as mean ± SEM (two- way ANOVA; **, p < 0.01; n = 3). Supplemental Figure S3. Targeting RBPJ does not affect non-BTIC proliferation. Non-BTICs (Top, 3691; Bottom, 4121) were transduced with shCONT, shRBPJ-1, or shRBPJ-2. Cell proliferation was measured by CellTiter-Glo. 42 Xie et al. Supplemental Figure S4. RBPJ induces transcriptional profiles in BTICs distinct from Notch activation. A. In parallel experiments, 3691 BTICs were either treated with DAPT (at either 5 μM or 10 μM) vs. vehicle control (DMSO) or transduced with shRBPJ vs. shCONT. RNA-Seq was performed and the results displayed as a heat map with normalization to the relevant control. -
Hormonal Regulation of Oligodendrogenesis I: Effects Across the Lifespan
biomolecules Review Hormonal Regulation of Oligodendrogenesis I: Effects across the Lifespan Kimberly L. P. Long 1,*,†,‡ , Jocelyn M. Breton 1,‡,§ , Matthew K. Barraza 2 , Olga S. Perloff 3 and Daniela Kaufer 1,4,5 1 Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720, USA; [email protected] (J.M.B.); [email protected] (D.K.) 2 Department of Molecular and Cellular Biology, University of California, Berkeley, CA 94720, USA; [email protected] 3 Memory and Aging Center, Department of Neurology, University of California, San Francisco, CA 94143, USA; [email protected] 4 Department of Integrative Biology, University of California, Berkeley, CA 94720, USA 5 Canadian Institute for Advanced Research, Toronto, ON M5G 1M1, Canada * Correspondence: [email protected] † Current address: Department of Psychiatry and Behavioral Sciences, University of California, San Francisco, CA 94143, USA. ‡ These authors contributed equally to this work. § Current address: Department of Psychiatry, Columbia University, New York, NY 10027, USA. Abstract: The brain’s capacity to respond to changing environments via hormonal signaling is critical to fine-tuned function. An emerging body of literature highlights a role for myelin plasticity as a prominent type of experience-dependent plasticity in the adult brain. Myelin plasticity is driven by oligodendrocytes (OLs) and their precursor cells (OPCs). OPC differentiation regulates the trajectory of myelin production throughout development, and importantly, OPCs maintain the ability to proliferate and generate new OLs throughout adulthood. The process of oligodendrogenesis, Citation: Long, K.L.P.; Breton, J.M.; the‘creation of new OLs, can be dramatically influenced during early development and in adulthood Barraza, M.K.; Perloff, O.S.; Kaufer, D. -
Cloud-Clone 16-17
Cloud-Clone - 2016-17 Catalog Description Pack Size Supplier Rupee(RS) ACB028Hu CLIA Kit for Anti-Albumin Antibody (AAA) 96T Cloud-Clone 74750 AEA044Hu ELISA Kit for Anti-Growth Hormone Antibody (Anti-GHAb) 96T Cloud-Clone 74750 AEA255Hu ELISA Kit for Anti-Apolipoprotein Antibodies (AAHA) 96T Cloud-Clone 74750 AEA417Hu ELISA Kit for Anti-Proteolipid Protein 1, Myelin Antibody (Anti-PLP1) 96T Cloud-Clone 74750 AEA421Hu ELISA Kit for Anti-Myelin Oligodendrocyte Glycoprotein Antibody (Anti- 96T Cloud-Clone 74750 MOG) AEA465Hu ELISA Kit for Anti-Sperm Antibody (AsAb) 96T Cloud-Clone 74750 AEA539Hu ELISA Kit for Anti-Myelin Basic Protein Antibody (Anti-MBP) 96T Cloud-Clone 71250 AEA546Hu ELISA Kit for Anti-IgA Antibody 96T Cloud-Clone 71250 AEA601Hu ELISA Kit for Anti-Myeloperoxidase Antibody (Anti-MPO) 96T Cloud-Clone 71250 AEA747Hu ELISA Kit for Anti-Complement 1q Antibody (Anti-C1q) 96T Cloud-Clone 74750 AEA821Hu ELISA Kit for Anti-C Reactive Protein Antibody (Anti-CRP) 96T Cloud-Clone 74750 AEA895Hu ELISA Kit for Anti-Insulin Receptor Antibody (AIRA) 96T Cloud-Clone 74750 AEB028Hu ELISA Kit for Anti-Albumin Antibody (AAA) 96T Cloud-Clone 71250 AEB264Hu ELISA Kit for Insulin Autoantibody (IAA) 96T Cloud-Clone 74750 AEB480Hu ELISA Kit for Anti-Mannose Binding Lectin Antibody (Anti-MBL) 96T Cloud-Clone 88575 AED245Hu ELISA Kit for Anti-Glutamic Acid Decarboxylase Antibodies (Anti-GAD) 96T Cloud-Clone 71250 AEK505Hu ELISA Kit for Anti-Heparin/Platelet Factor 4 Antibodies (Anti-HPF4) 96T Cloud-Clone 71250 CCA005Hu CLIA Kit for Angiotensin II -
Deficiency for the Cysteine Protease Cathepsin L Promotes Tumor
Oncogene (2010) 29, 1611–1621 & 2010 Macmillan Publishers Limited All rights reserved 0950-9232/10 $32.00 www.nature.com/onc ORIGINAL ARTICLE Deficiency for the cysteine protease cathepsin L promotes tumor progression in mouse epidermis J Dennema¨rker1,6, T Lohmu¨ller1,6, J Mayerle2, M Tacke1, MM Lerch2, LM Coussens3,4, C Peters1,5 and T Reinheckel1,5 1Institute for Molecular Medicine and Cell Research, Albert-Ludwigs-University Freiburg, Freiburg, Germany; 2Department of Gastroenterology, Endocrinology and Nutrition, Ernst-Moritz-Arndt University Greifswald, Greifswald, Germany; 3Department of Pathology, University of California, San Francisco, CA, USA; 4Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA and 5Ludwig Heilmeyer Comprehensive Cancer Center and Centre for Biological Signalling Studies, Albert-Ludwigs-University Freiburg, Freiburg, Germany To define a functional role for the endosomal/lysosomal Introduction cysteine protease cathepsin L (Ctsl) during squamous carcinogenesis, we generated mice harboring a constitutive Proteases have traditionally been thought to promote Ctsl deficiency in addition to epithelial expression of the invasive growth of carcinomas, contributing to the the human papillomavirus type 16 oncogenes (human spread and homing of metastasizing cancer cells (Dano cytokeratin 14 (K14)–HPV16). We found enhanced tumor et al., 1999). Proteases that function outside tumor cells progression and metastasis in the absence of Ctsl. As have been implicated in these processes because of their tumor progression in K14–HPV16 mice is dependent well-established release from tumors, causing the break- on inflammation and angiogenesis, we examined immune down of basement membranes and extracellular matrix. cell infiltration and vascularization without finding any Thus, extracellular proteases may in part facilitate effect of the Ctsl genotype. -
(LXR/NR1H3) Regulates Differentiation of Hepatocyte-Like Cells Via
Liver X receptor α (LXRα/NR1H3) regulates differentiation of hepatocyte-like cells via reciprocal regulation of HNF4α Kai-Ting Chen, Kelig Pernelle, Yuan-Hau Tsai, Yu-Hsuan Wu, Jui-Yu Hsieh, Ko-Hsun Liao, Christiane Guguen-Guillouzo, Hsei-Wei Wang To cite this version: Kai-Ting Chen, Kelig Pernelle, Yuan-Hau Tsai, Yu-Hsuan Wu, Jui-Yu Hsieh, et al.. Liver X recep- tor α (LXRα/NR1H3) regulates differentiation of hepatocyte-like cells via reciprocal regulation of HNF4α. Journal of Hepatology, Elsevier, 2014, 61 (6), pp.1276-1286. 10.1016/j.jhep.2014.07.025. hal-01072495 HAL Id: hal-01072495 https://hal.archives-ouvertes.fr/hal-01072495 Submitted on 8 Oct 2014 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. This is the author’s final draft post-refeering (post-print) Find more peer-reviewed articles on our open access repository: http://hal-univ-rennes1.archives-ouvertes.fr/ MANUSCRIPT ACCEPTED Liver X receptor a (LXRa/NR1H3) regulates differentiation of hepatocyte-like cells via reciprocal regulation of HNF4a Kai-Ting Chen1,2,3, Kelig Pernelle4, Yuan-Hau -
Supplemental Data Olig2-Regulated Lineage-Restricted Pathway Controls Replication Competence in Neural Stem Cells and Malignant
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Caltech Authors Neuron, Volume 53 Supplemental Data Olig2-Regulated Lineage-Restricted Pathway Controls Replication Competence in Neural Stem Cells and Malignant Glioma Keith L. Ligon, Emmanuelle Huillard, Shwetal Mehta, Santosh Kesari, Hongye Liu, John A. Alberta, Robert M. Bachoo, Michael Kane, David N. Louis, Ronald A. DePinho, David J. Anderson, Charles D. Stiles, and David H. Rowitch Figure S1. Olig1/2+/- Ink4a/Arf-/-EGFRvIII Gliomas Express Characteristic Morphologic and Immunophenotypic Features of Human Malignant Gliomas (A) Tumors exhibit dense cellularity and atypia. (B) Characteristic infiltration of host SVZ stem cell niche. (C) Although occasional tumors exhibited pseudopalisading necrosis (n, arrowhead) and hemorrhage (h, arrowhead) similar to human GBM (Astrocytoma WHO Grade IV), most tumors lacked these features. (D) IHC for hEGFR highlights hallmark feature of human gliomas, including perivascular (pv) and subpial (sp) accumulation of tumor cells, (E) striking white matter tropism of tumor cells in corpus callosum (cc), and (F) distant single cell infiltration of cerebellar white matter (wm, arrows). (G-J) Immunohistochemical markers characteristic of human tumors (Gfap, Olig2, Olig1, Nestin) are present. (K and L) Weak staining for the early neuronal marker TuJ1 and absence of the differentiated neuronal marker, NeuN similar to human glioma and consistent with heterogeneous lines of partial differentiation. Figure S2. Olig1/2+/- Ink4a/Arf-/-EGFRvIII Neurospheres Are Multipotent and Olig1/2-/- Ink4a/Arf-/-EGFRvIII Neurospheres Are Bipotent Olig1/2+/- or Olig1/2-/- Ink4a/Arf-/-EGFRvIII neurospheres were allowed to differentiate for 6 days in medium without EGF.